ArticleCancer metastasis reviews2018
Mitochondrial polymorphisms contribute to aging phenotypes in MNX mouse models.
Article in Cancer metastasis reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Mitochondrial tRNA-Derived Fragments as Candidate Metastasis-Modifying RNA.Cancer research communications · 2026Article
- Epithelial-to-mesenchymal transition (EMT) and cancer metastasis: the status quo of methods and experimental models 2025.Molecular cancer · 2025Review
- Multi-tissue metabolomics reveal mtDNA- and diet-specific metabolite profiles in a mouse model of cardiometabolic disease.Redox biology · 2025Article
- Pathogenic synergy: dysfunctional mitochondria and neuroinflammation in neurodegenerative diseases associated with aging.Frontiers in aging · 2025Review
- Article
- Generating Mitochondrial-Nuclear Exchange (MNX) Mice to Identify Mitochondrial Determinants of Cancer Metastasis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Roles of mitochondrial genetics in cancer metastasis.Trends in cancer · 2022Review
- Mechanisms of breast cancer metastasis.Clinical & experimental metastasis · 2022Review
- Differential accumulation of tau pathology between reciprocal F1 hybrids of rTg4510 mice.Scientific reports · 2021Article
- Mitohormesis, UPRCancer research · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Many inbred strains of mice develop spontaneous tumors as they age. Recent awareness of the impacts of mitochondrial DNA (mtDNA) on cancer and aging has inspired developing a mitochondrial-nuclear exchange (MNX) mouse model in which nuclear DNA is paired with mitochondrial genomes from other strains of mouse. MNX mice exhibit mtDNA influences on tumorigenicity and metastasis upon mating with transgenic mice. However, we also wanted to investigate spontaneous tumor phenotypes as MNX mice age. Utilizing FVB/NJ, C57BL/6J, C3H/HeN, and BALB/cJ wild-type inbred strains, previously documented phenotypes were observed as expected in MNX mice with the same nuclear background. However, aging nuclear matched MNX mice exhibited decreased occurrence of mammary tumors in C3H/HeN mice containing C57BL/6J mitochondria compared to wild-type C3H/HeN mice. Although aging tumor phenotypes appear to be driven by nuclear genes, evidence suggesting that some differences are modified by the mitochondrial genome is presented.
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Registered trials
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